So we've talked about angiotensin 2,
and we know that angiotensin 2 is a pretty small hormone.
It's only about 8 amino acids.
And so I'm going to draw it that way.
It's 8 little balls representing 1 amino acid
per tiny little ball-- almost like pearls on a necklace.
And they're floating through this blood vessel,
and they're headed to many different targets.
So these little molecules are headed to various organs.
And so let's talk about what those organs might be.
So one target for sure is the blood vessel.
So we have the blood vessel here.
And in the blood vessel wall, we have smooth muscle.
And the angiotensin hormone actually
gets that smooth muscle to constrict.
And so that's called vasoconstriction.
It's actually easy to remember this
because, if you think about the word "angiotensin,"
it's literally "angio" meaning blood vessel and "tensin" you
can think of making "tense."
So it's making the blood vessel tense and constrict down.
We know that, if you cause vasoconstriction,
you're going to actually increase resistance
because that's how resistance works in tubes.
And so if you're increasing resistance,
try to keep in mind that formula that we talked about way back
when for blood pressure-- delta P equals Q times R.
And now we're finally kind of seeing
how this formula is useful.
If we talk about P on the arterial side
minus P of the venous side.
That would be the change in pressure.
That would be delta P. And that equals Q.
And this Q is actually going to be a couple things.
It's going to stroke volume times heart rate.
And so that's the flow.
And all of that times resistance.
I should make this very clear so you're not
confused by what I'm writing here.
Sometimes my penmanship gets a little bit wacky.
This is your flow.
So you have this increase in resistance.
And you can see that, if I tell you
that your venous pressure over here
is really not going to change a whole heck of a lot
and if you can increase your resistance,
then you can definitely see how you
would increase your arterial pressure.
So it makes perfect sense using the formula.
And you can see now how angiotensin 2 accomplishes
that.
Oh, and actually, the last thing I
should mention before I move on is
that this is actually a pretty rapid response.
So very quickly the blood vessels
will start constricting if angiotensin 2 is around.
So now, another target organ would be the kidneys.
And so here's a little kidney here,
and this kidney is going to be affected by angiotensin 2
very slowly by comparison.
So it's actually more of a slow response.
And what actually happens is you get sodium reabsorption.
As the kidneys are reabsorbing the sodium,
they actually also pick up water.
So as the blood starts filling up
with more sodium and more water that you're not peeing out--
because you're, of course, reabsorbing it
from what would otherwise have been urine.
You end up having very concentrated urine,
and your blood ends up getting all the salt and water.
And your stroke volume goes up.
So your stroke volume increases.
And you can see from that equation
that we just drew that if your stroke volume goes up,
then again, your arterial blood pressure would go up
as well.
So here's a double check for that.
So now, if stroke volume goes up, aneurysms go up.
Your arterial pressure is definitely
going to start going up.
So angiotensin effects two different target organs.
And actually, it's not even done there.
It continues to affect other things.
It even has an effect on the pituitary gland.
So this is your pituitary gland.
And the pituitary gland is actually
in charge of releasing hormones of its own.
When it gets a signal from angiotensin 2,
it'll start sending off its own hormone called ADH.
And ADH is antidiuretic hormone.
It'll definitely cause vasoconstriction of the blood
vessels, just like angiotensin 2 did.
But instead of that sodium reabsorption,
this ADH actually causes water reabsorption.
Now, the effect for blood pressure in many ways
is going to be similar.
Because if you're reabsorbing water,
again, your stroke volume will go up.
And if your stroke volume goes up,
your arterial pressure goes up.
So at the end of the day, your pressure will still go up,
but it's slightly different because it's
water reabsorption versus salt reabsorption.
And we'll talk about the difference momentarily.
But before I get to that, the last target organ
I want to mention is another gland called the adrenal gland.
And the adrenal gland is literally sitting on top
of the kidneys, and that's why it's called "ad-renal."
And the adrenal gland is going to send off
its own hormone called aldosterone.
Aldosterone is going to affect the kidneys.
And just like the angiotensin 2, aldosterone
is going to cause salt reabsorption.
And that's the main kind of thing that it does.
And this salt reabsorption is going
to lead to more water absorption and increase in stroke volume.
So you can see how increase in resistance and increase
in stroke volume is how our body is
going to get our blood pressure back in control.
Now I want to talk about one thing
in a little bit more detail, which
is this whole salt versus water reabsorption issue.
So both of them increase stroke volumes.
So you might be wondering what is the difference
and why did I talk about the two separately.
So let me get to that now.
Let's do sodium, or salt, on this side.
I'll write sodium.
And on this side, I'll write water.
And we'll talk about sodium first.
So if you have your nephron here,
this is what's going to eventually lead to urine.
You have little cells here lining it,
and you have them on both sides.
I'm just going to focus on one side for simplicity.
And you have a blood vessel.
Let's say right here.
And so these cells are going to help to reabsorb stuff that's
otherwise going to go into the urine.
One strategy for getting water back--
let's say you want to reabsorb water, which
is what you want to do if you want to increase your blood
pressure-- one strategy for getting water back
would be to pull out salt.
Because you know that if you pull out salt through osmosis,
water is going to follow.
So that's a pretty good strategy-- getting water back.
That would work.
But the assumption-- and this is very, very important--
the assumption is that this barrier right here
is permeable to water.
And so if it is permeable to water,
then this sodium reabsorption strategy works.
Now, let's imagine for a second that you try this,
and it's actually not permeable to water.
What would happen?
Well, if you didn't have that permeability-- I'm
going to redraw it over here-- then, when you try
to bring the salt over-- and let's say you have your blood
vessel again over here-- you try to bring your salt over.
The moment that that water tries to follow,
it's going to bounce off.
It's going to do this and bounce right off.
It's not going to work.
You've got to try something different.
That's exactly what happens is that, in areas where you don't
have permeability to water-- so let's
say this is not permeable to water--
you need a new strategy.
And the strategy in a way is very, very simple.
It's, well, if it's not permeable to water,
why not forget about reabsorbing salt for the moment.
Why not just do something like this
and create little channels?
So that's exactly what happens.
You create these little channels,
and water can just go through it.
So basically, you make it permeable by creating channels.
And you say, OK.
Well, that's the better strategy for getting water in this case.
So if it's initially not permeable to water,
throw in a bunch of water channels and force that water--
or allow that water.
Maybe force is not the right word--
allow that water to get through using your own channels.
That's basically what the difference is.
So if you look at ADH versus the other two hormones--
aldosterone and angiotensin 2-- ADH
is using the water channel approach because here-- I'll
write it in red-- here where this works the water is usually
not permeable.
I mean, the nephron is not permeable normally to water.
And so that's why ADH throws in a bunch of water channels.
And aldosterone and angiotensin work
in areas of the nephron that are permeable to water.
That's why their salt strategy works pretty well.
But you can see now that, in both situations,
the key is getting water back-- either doing it through a salt
gradient or doing it through getting
a bunch of water channels in there.
In both situations, you increase your stroke volume.